Bronchial asthma
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Bronchial asthma is a chronic inflammatory disorder of the airways characterized by recurrent episodes of wheezing, breathlessness, chest tightness and coughing due to bronchospasm and airway obstruction. The symptoms are usually triggered by allergens, exercise, cold air or other stimuli and are at least partially reversible with treatment. It is caused by an inflammatory response in the airways mediated by TH2 cells and mast cells leading to increased mucus secretion, smooth muscle hypertrophy and bronchospasm. Common types include atopic asthma triggered by environmental allergens and non-atopic asthma triggered by respiratory infections.
Bronchial asthma
- 1. Bronchial Asthma Dr.CSBR.Prasad, M.D.
- 2. Bronchial asthma - gist
- 3. Bronchial asthma Disease characterized by increased responsiveness of the tracheobronchial tree to various stimuli, potentiating paroxysmal constriction of the bronchial tree.
- 4. Bronchial asthma Patients with asthma experience: 1. Attacks of severe dyspnea, coughing, and wheezing. 2. Rarely, “status asthmaticus” - may prove fatal. 3. Patients may be asymptomatic between the attacks. In some cases, the attacks are triggered by exercise and cold or by exposure to an allergen, but often no trigger can be identified. There has been a significant increase in the incidence of asthma in the Western world in the past three decades. In Bangalore 50% of children suffer from asthma. Air pollution is thought to be the main culprit.
- 5. Definition Chronic inflammatory disorder of airways that causes recurrent episodes of: – Wheezing – Breathlessness – Chest tightness & – Cough particularly at night and /or early morning
- 6. These symptoms are usually associated with wide spread but variable bronchoconstriction and air flow limitation that is at least partially reversible, either spontaneously or with treatment It is thought that inflammation causes increase in airway responsiveness (bronchospasm) to a variety of stimuli
- 7. Frequency and severity of symptoms 1. Mild, intermittent 2. Moderate 3. Severe, persistent
- 8. Clinical categories 1. Steroid dependent 2. Steroid resistant 3. Difficult 4. Brittle asthma
- 9. Informal categories 1. Seasonal 2. Exercise induced 3. Drug induced 4. Occupational asthma 5. Asthmatic bronchitis in smokers 6. Allergic bronchopulmonary aspergillosis
- 10. Typical categories 1. Extrinsic (allergic, reagin mediated, atopic) 2. Intrinsic (idiosyncratic) 3. Mixed (intrinsic and extrinsic factors operative)
- 11. Figure 15-10 A simplified scheme of the system of type 1 helper T (TH1) and type 2 helper (TH2) cells.
- 12. Structural alterations “Airway remodelling” • Smooth muscle proliferation • Subepithelial collagen deposition Mediated by: 1. Skewed TH2 differentiation 2. ADAM-33 gene abnormality 3. Mast cells
- 13. Figure 15-12 Comparison of a normal bronchiole with that in a patient with asthma.
- 14. Atopic / Allergic asthma • Most common type • Environmental agent: dust, pollen, food, animal dander • Family history - present • Serum IgE levels - increased • Skin test with offending agent –wheal flare
- 15. Two reactions Classic Ig E mediated hypersensitivity reaction has 2 responses 1. Acute immediate response 2. Late phase reaction
- 16. Figure 15-11 A model for allergic asthma.
- 17. Pathogenesis • Ag + presensitised IgE coated mast cells to same or cross reacting antigen • Chemical mediators • Mucosal surface • Submucosal mast cells • Direct stimulation of subepithelial vagal receptors • Minutes – Bronchoconstriction.
- 18. Primary mediators 1.Th2 cells > IL 4,5 > IgE production+EØ & Mast cell recruitment 2.Histamine - bronchconstriction by direct and cholinergic reflex actions 3.ECF and NCF
- 19. Secondary mediators LT C4, D4, and E4. prolonged bronchospasm increased vascular permeability increased mucus secretion. Prostaglandins (D2) Bronchospasm Vasodilation PAF platelet aggregation granule secretion.
- 20. Late phase reaction starts 4-8hrs later and persits for 12-24hrs Caused by recruitment of BØs, NØs, EØs • HRF – Histamine releasing factor • MBP – Major basic protein from EØs Direct epithelial damage • Neutrophils – inflammatory injury.
- 21. Non atopic asthma • Triggered by respiratory tract infection • Viruses - most common culprits • Family history uncommon • IgE level normal • No associated allergy • Skin tests NEGATIVE • Cause- hyperirritability of bronchial tree.
- 22. Drug induced asthma • Several pharmcologic agents • Aspirin sensitive asthma occurs in recurrent rhinitis nasal polyposis. • Increased bronchoconstrictor leukotrienes. Exqusitively sensitive to small doses of aspirin. • Inhibits COX pathway, without affecting LPO pathway
- 23. Allergic Bronchopulmonary Aspergillosis • Caused by spores of aspergillus fumigatus • Antigen challenge • Type I IgE induced reaction • 4 to 6 hr later Type III mediated response.
- 24. Occupational asthma • Fumes (epoxy resins, plastics) • Organic / chemical (dust, wood, cotton) • Gases (toluene) • Other chemicals (formaldehyde, penicillin) • Mechanism of injury: type I IgG mediated reactions liberation of bronchoconstrictors directly unknown hypersensitivity.
- 25. Morphology - gross • Lungs, over distended due to over inflation • Small areas of atelectasis • Occlusion of bronchi and bronchioles by thick tenacious mucous plugs.
- 26. These lungs appear essentially normal, but are the hyperinflated lungs of a patient who died with status asthmaticus.
- 27. This cast of the bronchial tree is formed of inspissated mucus and was coughed up by a patient during an asthmatic attack. The outpouring of mucus from hypertrophied bronchial submucosal glands, the bronchoconstriction, and dehydration all contribute to the formation of mucus plugs that can block airways in asthmatic patients.
- 28. Morphology - Micro • Mucous plugs-whorls of shed epithelium CURSHMANN’S SPIRALS • Numerous Eøs and CHARCOT-LEYDEN CRYSTALS • Crystalloids made of MBP.
- 29. Microscopy (Airway remodeling) • Thickening of BM of bronchial epithelium • Edema and infammatory infiltrate in bronchial walls with EØ (5 to 50 % ) • Increased in size of submucosal mucous glands • Hypertrophy of bronchial wall muscle.
- 30. Walk thru wheeze ? Walk thru angina ?
- 31. END
- 32. Contact: Dr.CSBR.Prasad, M.D., Associate Professor, Deptt. of Pathology, Sri Devaraj Urs Medical College, Kolar-563101, Karnataka, INDIA. CSBRPRASAD@REDIFFMAIL.COM